Activated myeloid dendritic cells release interleukin-12 (IL-12) and IL-23, which induce the proliferation of T-helper type 1 (Th1), Th17, and Th22 cells that subsequently produce pro-inflammatory cytokines (e.g., IL-17, IL-122, interferon gamma [IFN-γ], and tumor necrosis factor-alpha [TNF-α]) that characterize psoriasis, with the IL-23/Th17 pathway being the most predominant [2]. This evidence concerns the gene IL17A and psoriasis.